Evidence map›Paper›PMID 42657388›Full record

ArticleInternational journal of nanomedicine2026

Rg1-Loaded Tetrahedral DNA Nanostructures Attenuate Myocardial Ischemia-Reperfusion Injury by Suppressing Oxidative and Endoplasmic Reticulum Stress.

Fengxia Lin, Jiamei Huang, Zetao Chen, Fanjia Zhong, Luhua Xu, Na Liu, Miao Gan, Haoran Yin, Zhiwen Li, Xiaoduo Zhang and 7 more

Abstract read
In one paragraph

Article in International journal of nanomedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Fengxia Lin *Department of Cardiology, Shenzhen Bao'an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, People's Republic of China.ORCID 0000-0002-5549-738X
Jiamei Huang *Department of Cardiology, Shenzhen Bao'an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, People's Republic of China.ORCID 0009-0002-4432-4237
Zetao Chen *Department of Cardiology, Shenzhen Bao'an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, People's Republic of China.ORCID 0000-0003-4458-6915
Fanjia Zhong *Department of Cardiology, Shenzhen Bao'an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, People's Republic of China.ORCID 0009-0005-1374-6252
Luhua XuDepartment of Cardiology, Shenzhen Bao'an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, People's Republic of China.ORCID 0009-0004-0565-3446
Na LiuSchool of Traditional Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, Guangdong, People's Republic of China.
Miao GanDepartment of Cardiology, Shenzhen Bao'an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, People's Republic of China.
Haoran YinDepartment of Cardiology, Shenzhen Bao'an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, People's Republic of China.ORCID 0009-0003-7541-5454
Zhiwen LiDepartment of Cardiology, Shenzhen Bao'an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, People's Republic of China.
Xiaoduo ZhangDepartment of Cardiology, Shenzhen Bao'an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, People's Republic of China.
Yinzhi SongDepartment of Cardiology, Shenzhen Bao'an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, People's Republic of China.
Xi WangDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, People's Republic of China.
Hui ZhuoDepartment of General Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan, People's Republic of China.
Hongcai ShangKey Laboratory of Chinese Internal Medicine of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Sheng LinKey Laboratory of Chinese Internal Medicine of the Ministry of Education, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Zhicong ZengDepartment of Cardiology, Shenzhen Bao'an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, People's Republic of China.
Rongfeng YangDivision of Cardiovascular Intensive Care (CICU), Cardiac and Vascular Center, The University of Hong Kong-Shenzhen Hospital, Shenzhen, Guangdong, People's Republic of China.ORCID 0000-0002-3403-1951

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Myocardial ischemia-reperfusion injury (MIRI) remains a major clinical challenge in the management of acute myocardial infarction. Ginsenoside Rg1, a bioactive component from Methods: We designed a novel DNA nanocarrier, Rg1@pTDN, by loading Rg1 onto a tetrahedral DNA nanostructure (TDN) modified with the myocardial-targeting peptide CREKA. The physicochemical characteristics of Rg1@pTDN were evaluated by DLS, zeta potential analysis, AFM, and gel electrophoresis. Biodistribution, biosafety, and cellular uptake were assessed in vitro and in vivo. Cardioprotective efficacy was evaluated in a murine MIRI model and a H/R injury cell model. Mechanistic studies focused on oxidative stress and endoplasmic reticulum (ER) stress pathways. Results: Rg1@pTDN exhibited uniform nanoscale structure, high Rg1 loading efficiency, and good colloidal stability. In vivo imaging revealed preferential accumulation in cardiac tissue following intravenous administration. Rg1@pTDN was well tolerated and improved survival, cardiac function, and myocardial histology in MIRI mice. It significantly reduced serum CK-MB concentrations and oxidative stress markers (MDA), while increasing antioxidant enzyme activities (SOD, GSH-Px). In vitro, Rg1@pTDN suppressed ROS accumulation and H/R-induced apoptosis in H9c2 cells. Furthermore, Rg1@pTDN alleviated H/R-induced ER stress, as shown by decreased GRP78 and CHOP mRNA expression and reduced phosphorylated PERK and CHOP protein levels. Conclusion: Rg1@pTDN represents a promising nanotherapeutic strategy for myocardial ischemia-reperfusion injury through targeted delivery and dual inhibition of oxidative and ER stress. This DNA-based platform offers a versatile approach for enhancing the efficacy of natural compounds in cardiovascular disease.

Indexed as

DNA NanostructuresEndoplasmic Reticulum StressGinsenosidesMyocardial Reperfusion InjuryOxidative StressAnimalsDrug CarriersEndoplasmic Reticulum Chaperone BiPMaleMiceMice, Inbred C57BLMyocardiumDrug CarriersEndoplasmic Reticulum Chaperone BiPginsenoside Rg1GinsenosidesHspa5 protein, mouseendoplasmic reticulum stressginsenoside Rg1myocardial ischemia–reperfusion injuryoxidative stresstetrahedral DNA nanostructure

Identifiers

PMID42657388
PMCPMC13511464

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.